The present invention, in some embodiments thereof, relates to the field of cardiac medicine and more particularly but not exclusively to atrioventricular valve leaflet augmentation.
An aspect of some embodiments of the invention relates to improving the functioning of the mitral valve or the tricuspid valve. In the following, provided is a brief explanation of the structure of the mitral valve and its relation to the functioning of the heart in general. Afterwards, a brief explanation of mitral valve insufficiency and some treatments of this condition are described.
The Human Heart and the Mitral Valve
The human heart 10, depicted in cross sectional long axis view in FIG. 1, is a muscular organ that pumps deoxygenated blood through the lungs to oxygenate the blood and pumps oxygenated blood to the rest of the body by rhythmic contractions of four chambers.
After having circulated in the body, deoxygenated blood from the body enters the right atrium 12 through the vena cava 14. Right atrium 12 contracts, pumping the blood through a tricuspid valve 16 into the right ventricle 18. Right ventricle 18 contracts, pumping the blood through the pulmonary semi-lunar valve 20 into the pulmonary artery 22 which splits to two branches, one for each lung. The blood is oxygenated while passing through the lungs and reenters the heart to the left atrium 24.
Left atrium 24 contracts, pumping the oxygenated blood through the mitral valve 26 into the left ventricle 28. Left ventricle 28 contracts, pumping the oxygenated blood through the aortic semi-lunar valve 30 into the aorta 32. From aorta 32, the oxygenated blood is distributed to the rest of the body.
Physically separating left ventricle 28 and right ventricle 18 is interventricular septum 33. Physically separating left atrium 24 and right atrium 12 is an interatrial septum (25, FIG. 2b).
Mitral valve 26, depicted in FIG. 2A (top view) and in FIG. 2B (cross sectional long axis view) is defined by an approximately circular mitral annulus 34 that defines a mitral orifice 36. Attached to the periphery of mitral annulus 34 is an anterior leaflet 38 and a smaller posterior leaflet 40, leaflets 38 and 40 joined at commissures 41. Each leaflet is between about 0.8 and 2.4 mm thick and composed of three layers of soft tissue. The typical area of mitral orifice 36 in a healthy adult is between 4 and 6 cm2 while the typical total surface area of leaflets 38 and 40 is approximately 12 cm2. Consequently and as depicted in FIG. 2B, leaflets 38 and 40 curve downwards into left ventricle 28 and coapt to accommodate the excess leaflet surface area, producing a coaptation depthdepth 42 that constitutes a seal. The typical length of coaptation depthdepth 42 in a healthy heart 10 of an adult is approximately 7-8 mm.
The bottom surface of anterior leaflet 38 and posterior leaflet 40 are connected to papillary muscles 44 at the bottom of left ventricle 28 by posterior chordae 46 and anterior chordae 48.
During diastole, left atrium 24 contracts to pump blood downwards into left ventricle 28 through mitral valve 26. The blood flows through mitral orifice 36 pushing leaflets 38 and 40 downwards into left ventricle 28 with little resistance.
During systole left ventricle 28 contracts to pump blood upwards into aorta 32 through aortic semi-lunar valve 30. Mitral annulus 34 contracts pushing leaflets 38 and 40 inwards and downwards, reducing the area of mitral orifice 36 by about 20% to 30% and increasing the length of coaptation depthdepth 42. The pressure of blood in left ventricle 28 pushes against the bottom surfaces of leaflets 38 and 40, tightly pressing leaflets 38 and 40 together at coaptation depthdepth 42 so that a tight leak-proof seal is formed. To prevent prolapse of leaflets 38 and 40 upwards into left atrium 24, papillary muscles 44 contract pulling the edges of leaflets 38 and 40 downwards through posterior chordae 46 and anterior chordae 48, respectively.
Mitral Valve Insufficiency
As is clear from the description above, an effective seal of mitral valve 26 is dependent on a sufficient degree of coaptation, in terms of length, area and continuity of coaptation depth 42. If coaptation depth 42 is insufficient or non-existent, there is mitral valve insufficiency, that is, regurgitation of blood from left ventricle 28 up into left atrium 24. A lack of sufficient coaptation may be caused by any number of physical anomalies that allow leaflet prolapse (for example, elongated or ruptured chordae 46 and 48, weak papillary muscles 44) or prevent coaptation (for example, short chordae 46 and 48, small leaflets 38 and 40).
Mitral valve insufficiency leads to many complications including arrhythmia, atrial fibrillation, cardiac palpitations, chest pain, congestive heart failure, fainting, fatigue, low cardiac output, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, shortness of breath, and sudden death.
There are a number of pathologies that lead to a mitral valve insufficiency including collagen vascular disease, ischemic mitral regurgitation, myxomatous degeneration of leaflets 38 and 40 and rheumatic heart disease.
In ischemic mitral regurgitation (resulting, for example, from myocardial infarction, chronic heart failure), leaflets 38 and 40 and chordae 46 and 48 have normal structure and the mitral valve insufficiency results from altered geometry of left ventricle 28. As a result of ischemia, portions of the heart walls necrose. During healing, the necrotic tissue is replaced with unorganized tissue leading to remodeling of the heart which reduces coaptation through distortion of mitral annulus 34 and sagging of the outer wall of left ventricle 28 which displaces papillary muscles 44.
In FIGS. 3A (top view) and 3B (cross sectional long axis view), The reduction of coaptation resulting from ischemia is depicted for a mitral valve 26 of an ischemic heart 50 that has undergone mild remodeling and suffers from ischemic mitral regurgitation. In FIG. 3B is seen how an outer wall of left ventricle 28 sags outwards, displacing papillary muscles 44 downwards which, through chordae 46 and 48, pulls leaflets 38 and 40 downwards and apart, reducing coaptation. The incomplete closure of mitral valve 26 is seen in FIGS. 3A and 3B.
In some cases, the following progression is observed. Initially, ischemic mitral regurgitation is a minor problem, typically leading only to shortness of breath during physical exercise due to the fact that a small fraction of blood pumped by left ventricle 28 is pumped into left atrium 24 and not through aortic semi-lunar valve 30, reducing heart capacity. To compensate for the reduced capacity, left ventricle 28 beats harder and consequently remodeling continues. Ultimately leaflet coaptation is entirely eliminated as leaflets 38 and 40 are pulled further and further apart, leading to more blood regurgitation, further increasing the load on left ventricle 28, and further remodeling. Ultimately, the left side of the heart fails and the person dies.
Apart from humans, mammals that suffer from mitral valve insufficiency include horses, cats, dogs, cows and pigs.
Currently, it is accepted to use open-heart surgical methods to improve mitral valve functioning by many different methods including: modifying the subvalvular apparatus (for example, lengthening the chordae) to improve coaptation; by implanting an annuloplasty ring, (for example, as described in U.S. Pat. Nos. 3,656,185, 6,183,512 and 6,250,308) to force mitral valve annulus 34 into a normal shape; or by implanting devices in the mitral valve to act as prosthetic leaflets (for example, the United States Patent applications published as US 2002/065554, US 2003/0033009, US 2004/0138745 or US 2005/0038509).
Surgical augmentation of a mitral valve anterior leaflet 38 for improving mitral valve leaflet coaptation for treating ischemic mitral valve regurgitation is taught by Kincaid E H, Riley R D, Hines M H, Hammon J W and Kon N D in Ann. Thorac. Surg. 2004, 78, 564-568. First, an incision is made in the anterior leaflet almost from commissure to commissure. The edges of a roughly elliptical patch of material (for example, bovine pericardium, 1 cm wide by 3 cm long) are sutured to either side of the incision augmenting the anterior leaflet by an amount roughly equal to the surface area of the patch. Additionally, a flexible annuloplasty ring is implanted to reshape the mitral annulus. Although possibly effective, such augmentation is considered a complex surgical procedure performed only by cardiac surgeons having above average skill.
Open heart surgery of any kind is complex, requires long recovery time and is accompanied by a high rate of complications and death. The failure rate of operations for mitral valve function improvement is unacceptably high. Even when successfully performed, persons having undergone such surgeries have an increased chance of infection and stroke, and are often required to use anticoagulant agents for the rest of their lives. Often there is a need to repeat the surgery after a few years.
For these reasons, such procedures are usually tried only when the degree of mitral valve insufficiency is such that death is likely or imminent.
Following a myocardial infarction, the one-year mortality of persons with no ischemic mitral regurgitation is about 6%, with mild ischemic mitral regurgitation about 10%, with moderate ischemic mitral regurgitation about 17% and with severe ischemic mitral regurgitation approximately 40%.